Effect of serum on diesel exhaust particles (DEP)-induced apoptosis of airway epithelial cells in vitro

Abstract

Patients with chronic airway diseases may be more susceptible to adverse effects of air pollutants including diesel exhaust particles (DEP). We investigated effects of foetal calf serum (FCS) on DEP-induced changes in airway epithelial cell apoptosis and inflammation. DEP (50–200μg/ml) increased A549 cell viability in the absence of FCS. In the presence of 3.3%FCS, DEP (50–400μg/ml) decreased A549 cell viability. N-acetylcysteine (NAC, 33mM) and the c-jun N-terminal kinase (JNK) inhibitor (SP600125, 33μM) further decreased the viability in the presence of DEP (200μg/ml) and 3.3% FCS. Under serum-free (SF) condition, DEP (50μg/ml) reduced apoptotic cells; however, when 3.3% FCS added to the culture medium, this effect was abolished. DEP (200μg/ml) induced mRNA expression of p21CIP1/WAF1 both in absence or presence of 3.3% FCS and enhanced JNK2 mRNA expression only in the presence of 3.3% FCS. Under SF condition, DEP (50μg/ml) induced mRNA expression for p27 and p53, whereas cyclin E mRNA expression was inhibited by DEP (50 and 200μg/ml). Furthermore, DEP (200μg/ml) decreased the release of interleukin (IL)-8 in the absence of FCS. In conclusion, FCS modulates effects of DEP on cell death, cell cycle and apoptosis regulating proteins, and IL-8 release by activating oxidant stress pathways, JNK and NF-κB. Extravasation of serum, as occurs in the inflamed airways of patients with chronic airway diseases such as asthma and COPD, may render airway epithelial cells more susceptible to the deleterious effects of DEP.